Hyperphagia, or overeating and consequent obesity, is a long standing behavioral problem encountered among individuals of our society. The proposed model system offers pharmacological modification of feeding behavior coupled inexorably to defined physiological and morphological changes in the Satiety Center of the ventromedial hypothalamus. These characteristics permit the integration and correlation of structural and pharmacological techniques in the study of feeding behavior and its control. The Satiety center of the mouse ventromedial hypothalamus regulates feeding behavior. Gold-thioglucose (GTG) administration decouples this regulation with resultant hyperphagia, weight again, and subsequent obesity. GTG is presumed to act upon receptive neurons in the satiety center, and in fact, necrotizing doses of GTG induce the formation of macro lesions in the ventromedial hypothalamus suggesting destruction of the receptive neurons. Desensitizing doses of GTG on the other hand do not affect feeding behavior but cause lesions observable only with microscopic techniques. Observations of lesion development in the mouse ventromedial hypothalamus following GTG administration may be used to identify the GTG sensitive cells and thereby localize the neurons of the Satiety center. This study will involve the use of GTG as a pharmacological probe to identify and morphologically characterize the GTG sensitive neurons which are presumed to comprise the Satiety center. A mapping study involving combined light electron microscopy will be carried out in an attempt to characterize the neuroanatomy of the Satiety center. Reconstruction of Satiety center morphology from serial images will assist tracing of neuronal regulatory circuits involved in control of feeding behavior and obesity. A concurrent study of lesion pathology will be conducted to determine the sequence of morphological events leading to lesion formation, including microlesion development in response to desensitizing doses of GTG as well as the development of the more gross lesion resulting from necrotizing doses of GTG.